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Background :  Antimalarial drug resistance is a major challenge hampering malaria control and elimination.  Plasmodium falciparum , the leading causative parasite species, has developed resistance to basically all antimalarials. Continued surveillance of drug resistance using genetic markers provides important molecular data for treatment policies. This study sought to verify the genetic mechanism of resistance to sulfadoxine-pyrimethamine and assess the occurrence of point mutations associated with artemisinin resistance in  P. falciparum  clinical isolates from Eritrea.Methods :  Nineteen dried blood spot samples were collected from patients visiting Adi Quala, Keren and Gash Barka Hospitals, Eritrea. The patients were followed up after receiving treatment with first line artesunate-amodiaquine. Nested polymerase chain reaction and Sanger sequencing techniques were employed to genotype point mutations in the  P. falciparum  bifunctional dihydrofolate reductase-thymidylate synthase ( Pfdhfr , PF3D7_0417200), dihydropteorate synthase ( Pfdhps , PF3D7_0810800) and kelch 13 ( PfK13 , PF3D7_1343700) genes.Results :  Eight of nineteen (42%) of the dried blood spot samples were successful for PCR-amplification. Data analyses of the PCR-positive isolates revealed the following point mutations:  Pfdhfr  N51I in four isolates, C59R in one isolate, S108N in four isolates, a rare non-synonymous substitution V45A in four isolates and  Pfdhps  K540E in four isolates. No  PfK13  point mutations were reported.Conclusions :   Pfdhfr  C59R and  Pfdhps  K540E point mutations are reliable markers for the sulfadoxine-pyrimethamine quintuple mutant haplotype combination. These findings highlight first reports in Eritrea, which verify the underlying genetic mechanism of antifolate resistance. Continuous monitoring of the  PfK13  marker is recommended.

Screening for antifolate and artemisinin resistance in Plasmodium falciparum clinical isolates from three hospitals of Eritrea